Bone and Joint Center, VA Palo Alto Health Care System, USA.
J Biomech. 2011 Aug 11;44(12):2307-12. doi: 10.1016/j.jbiomech.2011.04.014. Epub 2011 Jul 7.
Meniscectomy is a significant risk factor for osteoarthritis, involving altered cell synthesis, central fibrillation, and peripheral osteophyte formation. Though changes in articular cartilage contact pressure are known, changes in tissue-level mechanical parameters within articular cartilage are not well understood. Recent imaging research has revealed the effects of meniscectomy on the time-dependent deformation of physiologically loaded articular cartilage. To determine tissue-level cartilage mechanics that underlie observed deformation, a novel finite element modeling approach using imaging data and a contacting indenter boundary condition was developed. The indenter method reproduces observed articular surface deformation and avoids assumptions about tangential stretching. Comparison of results from an indenter model with a traditional femur-tibia model verified the method, giving errors in displacement, solid and fluid stress, and strain below 1% (RMS) and 7% (max.) of the absolute maximum of the parameters of interest. Indenter finite element models using real joint image data showed increased fluid pressure, fluid exudation, loss of fluid load support, and increased tensile strains centrally on the tibial condyle after meniscectomy-patterns corresponding to clinical observations of cartilage matrix damage and fibrillation. Peripherally there was decreased consolidation, which corresponds to reduced contact and fluid pressure in this analysis. Clinically, these areas have exhibited advance of the subchondral growth front, biological destruction of the cartilage matrix, cartilage thinning, and eventual replacement of the cartilage via endochondral ossification. Characterizing the changes in cartilage mechanics with meniscectomy and correspondence with observed tissue-level effects may help elucidate the etiology of joint-level degradation seen in osteoarthritis.
半月板切除术是骨关节炎的一个重要危险因素,涉及细胞合成、中央纤维化和外周骨赘形成的改变。虽然关节软骨接触压力的变化是已知的,但关节软骨内组织水平机械参数的变化还不太清楚。最近的成像研究揭示了半月板切除术对生理负荷关节软骨时变变形的影响。为了确定导致观察到的变形的组织水平软骨力学,开发了一种使用成像数据和接触压痕边界条件的新有限元建模方法。压痕方法再现了观察到的关节表面变形,避免了对切向拉伸的假设。压痕模型的结果与传统的股骨-胫骨模型的比较验证了该方法,使位移、固体和流体应力以及感兴趣参数的应变的误差低于 1%(RMS)和 7%(最大值)。使用真实关节图像数据的压痕有限元模型显示,半月板切除术后胫骨髁中央的流体压力增加、流体渗出、流体负荷支撑丧失以及拉伸应变增加,这些模式与软骨基质损伤和纤维化的临床观察相对应。在周围区域,固结减少,这与本分析中接触和流体压力的减少相对应。临床上,这些区域表现为软骨下生长前沿的推进、软骨基质的生物破坏、软骨变薄以及最终通过软骨内成骨替代软骨。描述半月板切除术后软骨力学的变化及其与观察到的组织水平效应的对应关系,可能有助于阐明骨关节炎中关节水平退化的病因。